Influx And Efflux Are Coordinately Regulated

In the process of evolution of the ion-transport system, it was necessary to evolve specificity of the transporters. The occurrence of influx and efflux transporters for the same metal ion necessitated evolution of not only a specialized but also a highly regulated system. For a cell exposed to toxic metal ions, like Hg2+, Cu2+, Cd2+, or oxyanions of arsenic and antimony, it is obligatory to maintain the cytosolic ion concentration below the toxic level. In general, the cells survive the toxic ion effect with the aid of a specific ion-efflux system. Thus, for a nonessential but toxic ion, the necessity and advantage of simultaneously operating an uptake- and an efflux-transport system associated in several metal ion resistance operons remains speculative. In many instances, however, cells had evolved a transport system for a particular essential ion that can be used by a structurally similar toxic ion to enter the bacterial cell.

One can also advocate that metabolic penalty for having uptake pumps more specific is greater than the genetic cost of having plasmid genes in the population that can spread when needed [2]. Thus, most of the toxic metal (or metalloid) resistance is encoded by mobilizable extrachromosomal replicons or transposons. Among the known resistance systems, mercury, cadmium (along with zinc, cobalt, and nickel), and arsenic (along with antimony) resistance genetic determinants have been well characterized. All these toxic metal ion resistance operon systems, except the ars operon, are common in having coordinated regulation with the specific gene(s) for the ion-uptake system associated with the plasmid encoded resistance operon or encoded by the genome [324].

Mutation in the resistance gene of the operon causes hypersensitivity if the associated uptake gene(s) remains unaltered. In the mercury resistance (mer) operon, at least three genes merTPC are cotranscribed with merA and specify Hg2+ uptake system. Thus, the mer operon, lacking merA gene, which encodes the mercuric reductase to convert mercuric ion to volatile mercury, resulted in more hypersensitivity to Hg2+ than the isogenic strains lacking mer operon [325]. This observation, in fact, had helped to identify the mercuric ion uptake genes merTPC of the mer operon [47].

Similarly, a copCD clone of copper resistance copABCD [2] operon was phenotypically hypersensitive to copper [326]. Unlike mercuric ion, copper (or zinc) is an essential element but toxic at a higher level; thus, a homeostasis condition is maintained to ensure that the cells do not become copper (or zinc) depleted or copper (or zinc) surfeited [194]. Thus, complex and distinct operon systems having certain coordination between metabolism of these metals including uptake and resistance including efflux (and or binding) were evolved.

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